Feed

Anticancer therapy can eliminate immune-visible tumour cells while simultaneously imposing selective pressures that favour residual immune-evasive populations. This mini-review conceptualizes therapy-induced immunoediting as a dynamic continuum comprising pre-existing escape, therapeutic immune activation, a selective bottleneck, residual equilibrium and secondary escape. We discuss how genetic alterations, therapy-resistant stem-like tumour-cell states and spatial remodelling of vascular, stromal and myeloid niches cooperate to reduce tumour visibility, effector susceptibility and immune-cell access. Representative approved and investigational therapies illustrate both successful pharmacological interception and the limitations of non-selective immune intensification. We further highlight residual equilibrium as a clinically actionable window that may be identified through longitudinal tissue sampling, circulating tumour DNA and spatial or single-cell profiling. Clinically, longitudinal biomarkers may identify residual equilibrium and guide mechanism-matched treatment adaptation before immune-evasive populations expand into radiographically evident relapse.